Although antigen targets for ALL (CD19, CD22) and AML (CD33, CD123) could be useful for treating infant leukemia (20, 21), there are limitations to their use, including the development of lineage switching as an escape mechanism, especially in cells with KMT2A-r, in addition to the difficulty of apheresis and the subsequent manufacturing of CAR-T cells in infants (22, 23). This evidence concerns the gene CD22 and acute myeloid leukemia.